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Macrophage targeting in cancer.

Martha Lopez-Yrigoyen1, Luca Cassetta1, Jeffrey W Pollard1

  • 1MRC Centre for Reproductive Health, Queen's Medical Research Institute, The University of Edinburgh, Edinburgh, United Kingdom.

Annals of the New York Academy of Sciences
|May 24, 2020
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Tumor-associated macrophages (TAMs) can either fight or promote cancer. Reprogramming TAMs offers a promising strategy to enhance antitumor immunity and improve cancer therapy outcomes.

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TAMcancermacrophagereprogrammingtargetingtumor microenvironment

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Area of Science:

  • Immunology
  • Oncology
  • Cancer Biology

Background:

  • Tumor-associated macrophages (TAMs) are key immune cells in the tumor microenvironment (TME).
  • TAMs can exhibit dual roles, initially promoting antitumor responses but later adopting an immunosuppressive phenotype that drives tumor progression and therapy resistance.
  • Current TAM-targeting strategies like depletion or recruitment inhibition show limited efficacy.

Purpose of the Study:

  • To review the multifaceted roles of TAMs in cancer therapy.
  • To discuss the immunosuppressive properties of TAMs and their impact on immunotherapies.
  • To highlight emerging TAM-reprogramming strategies for cancer treatment.

Main Methods:

  • Literature review of TAM roles in tumorigenesis.
  • Analysis of TAM-targeting strategies in preclinical and clinical studies.
  • Discussion of TAM reprogramming as a therapeutic approach.

Main Results:

  • TAMs' phenotype shifts from antitumor to protumorigenic due to tumor evolution and TME changes.
  • TAMs contribute to tumor progression, metastasis, and therapeutic resistance.
  • Reprogramming TAMs to restore antitumor activity is a developing therapeutic strategy.

Conclusions:

  • Targeting TAMs is crucial for effective cancer therapy.
  • Reprogramming TAMs holds significant potential for enhancing antitumor immune responses.
  • Emerging strategies focus on modulating TAMs for improved cancer treatment outcomes, including in combination with immunotherapies.